title: Spatial learning and memory function-related gene expression in the hippocampus of mouse exposed to nanoparticle-rich diesel exhaust.
abstract: Diesel exhaust particles are a major constituent of ambient particulate matter, and most particles emitted directly from diesel exhaust are smaller than 1microm in diameter. Recently, the toxicity of diesel engine-derived nanoparticles has come to be recognized as an emerging social issue. In the present study, we investigated spatial learning ability and memory function-related gene expressions in mouse hippocampus after the exposure of animals to nanoparticle-rich diesel exhaust (NRDE) with or without a bacterial cell wall component. Lipoteichoic acid (LTA), a cell wall component derived from Staphylococcus aureus, was used to induce systemic inflammation. Male BALB/c mice were exposed to clean air (particle concentration, 4.58microg/m(3)) or NRDE (148.86microg/m(3)) for 5h per day on 5 days of the week for 4 weeks in an exposure chamber, with or without the weekly intraperitoneal injection of LTA. On the day after the final day of exposure, we used a Morris water maze apparatus to examine the ability of the animals to perform a spatial learning task. After the completion of the test, the animals were sacrificed and the hippocampus was collected from each mouse; the expressions of NMDA receptor subunits (NR1, NR2A and NR2B), proinflammatory cytokines (IL-1beta and TNF-alpha) and the oxidative stress marker heme oxygenase 1 were then investigated using real-time RT-PCR. In the Morris water maze task, NRDE/LTA (+) group took a longer time to reach the hidden platform than clear air/LTA (-) group. However, NRDE exposure alone did not affect it. The relative mRNA levels of the NMDA receptor subunits and proinflammatory cytokines were higher in hippocampus of NRDE/LTA (+) group compared to clear air/LTA (-) group. These results indicate that co-exposure of NRDE and LTA could affect spatial learning and memory function-related gene expressions in mouse hippocampus.
authors.affiliation: National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, Ibaraki 305-8506, Japan.
authors.forename: Tin-Tin
authors.initials: TT
authors.lastname: Win-Shwe
authors.forename: Shoji
authors.initials: S
authors.lastname: Yamamoto
authors.forename: Yuji
authors.initials: Y
authors.lastname: Fujitani
authors.forename: Seishiro
authors.initials: S
authors.lastname: Hirano
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Fujimaki
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects*; D051597:Hippocalcin / Q000187:drug effects*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D018782:Maze Learning / Q000187:drug effects; D008568:Memory / Q000187:drug effects*; D051379:Mice; D008807:Mice, Inbred BALB C; D053758:Nanoparticles / Q000633:toxicity*; D012333:RNA, Messenger / Q000378:metabolism; D011930:Reaction Time / Q000187:drug effects; D017470:Receptors, Glutamate / Q000235:genetics / Q000378:metabolism; D013037:Spatial Behavior / Q000187:drug effects*; D013682:Teichoic Acids / Q000494:pharmacology; D013997:Time Factors; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D016207:Cytokines; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D017470:Receptors, Glutamate; D013682:Teichoic Acids; D001335:Vehicle Emissions; D051597:Hippocalcin; C009900:lipoteichoic acid